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J.Health Sci., 51(1), 41-47, 2005
Deficits in the Brain Growth in Rats Induced by Methylmercury Treatment during the Brain Growth Spurt
Huan Sheng Pan,a Mineshi Sakamoto,*, b Xiao Jie Liu,b and Makoto Futatsukaa
aDepartment of Public Health, Graduate School of Medical and Pharmaceutical Sciences, Kumamoto University 1-1-1 Honjo, Kumamoto 860-8556, Japan amd bNational Institute for Minamata Disease, 4058-18 Hama, Minamata City, Kumamoto 867-0008, Japan
This paper describes the deficits in brain regional growth of rats treated with methylmercury (MeHg) among the postnatal developing phases. Rats were orally administered 10 mg/kg/day of methylmercury chloride (MMC) for 10 consecutive days from postnatal days 1 (PD-1), -14 and -35, which corresponded to the early-, late- and post-brain growth spurt, respectively. Weight-matched control rats were periodically isolated from their mother or diet and placed in an incubator for intervals of 4 to 10 hr in order to adjust the body weight to MMC-treated rats. The earlier the postnatal phase the higher the resistance to body weight loss induced by MMC. The rats were dissected on the day after final MMC treatment and the weight of organs and their mercury (Hg) concentrations were measured. Hg accumulation in the brain on the day after final treatment with 10 mg/kg/day of MMC was highest in the rats treated during the late-brain growth spurt. On the other hand, Hg accumulations in the liver and kidney increased rapidly with development of postnatal phases. Then, the brain/kidney and brain/liver ratio of Hg concentration were much higher in early postnatal rats than in later one. The weight of brain regions in MMC-treated rats was compared with those in weight-matched control rats. The significantly lower weight of the cerebrum, cerebellum and midbrain + diencephalon were confirmed in rats treated with MMC during the early-brain growth spurt. The significantly lower cerebellum weight was confirmed in rats treated with MMC during the late-brain growth spurt. The Significant differences were not observed in the brain regions in rats treated during post-brain growth spurt. In the case of human, a similar reduction of the brain weight occurred in the fetal and non-fetal infantile Minamata disease patients. The experiment using postnatal rats succeeded to reproduce the deficit in the brain growth during the early- and late brain growth spurt by MMC treatment.
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